(Circulation. 1995;91:284-290.)
© 1995 American Heart Association, Inc.
Articles |
From the Department of Epidemiology and Health Promotion (V. Salomaa), National Public Health Institute, Helsinki, Finland; Division of Hematology (V. Stinson, K.K.W.), University of Texas (Houston); Hadassah School of Public Health (J.D.K.), Hebrew University, Jerusalem, Israel; Division of Epidemiology (A.R.F.), School of Public Health, University of Minnesota (Minneapolis); and Collaborative Studies Coordinating Center (C.E.D.), Department of Biostatistics, University of North Carolina at Chapel Hill.
Correspondence to Kenneth K. Wu, MD, Professor and Director, Division of Hematology, University of Texas Medical School at Houston, 6431 Fannin, MSB 5.016, Houston, TX 77030.
Background Thrombosis, provoked by a rupture of an atherosclerotic plaque, plays a crucial role in precipitating a coronary heart disease event. Its role at the early stage of atherosclerosis has, however, been unclear, but it has been hypothesized that thrombosis or defective fibrinolysis contributes to the progression of atherosclerotic lesions.
Methods and Results We studied the association of plasminogen
activator inhibitor antigen (PAI-1), tissue-type plasminogen activator
antigen (TPA), and D-dimer with early atherosclerosis in a
cross-sectional case-control study involving 457 pairs chosen from the
biracial cohort of the Atherosclerosis Risk in Communities (ARIC)
Study. As examined by B-mode ultrasound, patients (cases) had
intima-media thickness of carotid arteries above the 90th percentile
and control subjects had thickness below the 75th percentile of the
ARIC cohort. Persons with a history of heart disease, stroke, or
claudication were excluded from the case-control selection. PAI-1, TPA,
and D-dimer were higher in patients than in control subjects
(P
.001, Wilcoxon signed rank statistic). In conditional
logistic regression analyses, the odds ratios of carotid
atherosclerosis were, for PAI-1, for example, 1.22, 1.54, and 1.60 in
the second, third, and fourth quartiles compared with the first
quartile (P<.0001, test of linear trend, adjusting for age,
systolic blood pressure, total cholesterol, acetylsalicylic acid use,
and time of blood draw). Corresponding tests for D-dimer and TPA also
showed an increasing trend (P<.0001).
Conclusions The findings support the hypothesis that thrombosis and fibrinolysis play a role at the early stage of the atherosclerotic process.
Key Words: thrombosis blood cells coagulation atherosclerosis
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